Although bright light is an effective treatment for Seasonal affective disorder, the mechanism of its actions remains unknown, as do the fundamental biological abnormalities responsible for the syndrome. We have been pursuing the pathophysiology of SAD along two lines: one involving optical information processing and the other involving neuroendocrine profiles. We have found that the effects of light treatment appear to be mediated by the Cm rather than the skin. In addition, the green wavelengths seem to be especially effective. We have found that patients with wintertime SAD are abnormally-sensitive in adapting to dim light. Taken together, these studies suggest that the eye may play a central role in winter SAD. Dopamine is an important neurotransmitter in retinal transmission and there is evidence of central dopaminergic abnormalities in SAD. Over the past year, therefore, we have focused our biological mechanisms of SAD research upon retinal pathophysiology in general and dopaminergic mechanisms in particular. In concert with a clinical trial of a dopaminergic precursor we examined various parameters of retinal physiology (electroretinograms and visual evoked potentials) in SAD patients and in normal controls. We have also continued our examination of dark adaptation in SAD patients in summer and winter. Two findings have emerged. First, abnormally delayed electroretinogram b-waves in response to pattern stimuli are seen in depressed SAD patients as compared with normal controls, an abnormality reminiscent of Parkinson's Disease. This raises the possibility of a retinal dopaminergic abnormality in SAD. Second, the supersensitive adaptation to dim light in SAD patients appears to persist in summer and thus be a trait marker for the syndrome. We have previously shown that the hypothalamo-pituitary-adrenal (HPA) "stress-response" axis is abnormal in patients with SAD and that light therapy corrects this abnormality. We followed up this finding this past year by investigating whether light enhances HPA axis functioning in normal controls and whether there is evidence of hypothalamo-pituitary-thyroid (HPT) axis abnormalities in SAD. Both of these lines of investigation yielded negative results.